Dietary Fibers in Inflammatory Bowel Diseases: History
View Latest Version
Please note this is an old version of this entry, which may differ significantly from the current revision.
Contributor:
Claudia Di Rosa
,
Annamaria Altomare
,
Elena Imperia
,
Chiara Spiezia
,
Yeganeh Manon Khazrai
,
Michele Pier Luca Guarino

Inflammatory bowel diseases (IBDs) are chronic, progressive, immune-mediated diseases of the intestinal tract. The main subtypes of IBDs are Chron’s disease (CD) and ulcerative colitis (UC). The etiology is still unclear, but there are genetic, environmental and host-related factors that contribute to the development of these diseases. Recent literature has shown that dietary therapy is the cornerstone of IBD treatment in terms of management of symptoms, relapse and care of the pathology. IBD patients show that microbiota dysbiosis and diet, especially dietary fiber, can modulate its composition. These patients are more at risk of energy protein malnutrition than the general population and are deficient in micronutrients. So far, no dietary component is considered responsible for IBD and there is not a specific therapeutic diet for it. 

  • inflammatory bowel disease
  • dietary fibers
  • nutrition

1. Introduction

Inflammatory bowel diseases (IBDs) are chronic, progressive, immune-mediated diseases of the intestinal tract [1] characterized by a progressing or relapsing and remitting disease course [2]. They are associated with significant morbidity, disability, and risk of complications [1] such as abdominal abscesses, fistulae, strictures and subsequent bowel obstruction, and an increased risk of gastrointestinal (GI) cancer [2]. To date, the etiology of these diseases is still not clear [3][4]; nevertheless, it is known that there are genetic [5][6][7][8][9][10][11][12][13][14][15][16][17], host-related [18][19][20][21][22] and environmental [16][19][23] factors that contribute to the development of gut inflammation and IBD (Table 1).
Table 1. Etiopathogenetic factors and its effects on IBD patients.
Etiopathogenetic Factors Effects
Genetic factors NOD2 gene mutation [5][6][7][8][9][10][11] Alteration of intestinal immune homeostasis and components which maintain the mucus layer
ATG16L1 gene mutation [5][6][12][13][14][15] Paneth cell function in autophagy mechanisms is compromised, so protection against infection removing many intracellular microbes is reduced
Locus IBD5 alteration [16][17] Wrong codification of a group of cationic organic transporters, OCTN1 and OCTN2. Reduction in cells and tissues from oxidative and/or inflammatory damage
Locus IBD3 alteration [16] Wrong codification of Major Histocompatibility Complex (MHC)
Host-related factors Microbiota alteration [18][19] Lower production of anti-inflammatory and immunoregulatory metabolites, in particular butyrate—a lack of which may contribute to increased intestinal inflammation
Immune response [18][20][21][22] Hyperactivity of T cells with excessive production of cytokines, among which IL-12, il-23 and IFN-γ promote a TH1 and TH17 lymphocytic phenotype. The inhibition of the effector cytokines, such as TNF-α
Environmental factors Diet [19][23] Red meat consumption has a pro-inflammatory effect. A high consumption of total fatty acids, polyunsaturated fatty acids (PUFAs), especially omega 6 fatty acids, increases the risk of developing both UC and CD
Cigarette smoking [16] Formation of fistulas and intestinal strictures increases the frequency of exacerbations and favors post-surgical relapses in CD. On the contrary, in UC, it seems to have a protective action and it is associated with less frequent flare-ups of the disease
The main subtypes of IBDs are Crohn’s disease (CD) and ulcerative colitis (UC) [4]. CD inflammation affects the whole intestine but the most common sites are in the small and large intestine (especially in the ileum) and perianal region and are classified as “L1: ileal-type”, “L2: colonic-type”, “L3: ileocolonic-type” and “L4: isolated upper disease” [20]. UC, on the other hand, is classified as: E1 ulcerative proctitis, when the site of the disease is limited to the rectum; E2 distal UC, when it is limited to a portion of the colorectal distal to the splenic flexure; and E3 extensive UC or pancolitis, when it extends from proximal to the splenic flexure [24]. The severity of IBD is classified as “remission”, “mild”, “moderate”, or “severe” based on clinical symptoms, signs, and blood tests [24]. Signs and symptoms of CD and UC are presented in Table 2.
Table 2. Symptoms and signs of CD vs. UC [25][26][27].
Symptoms and Signs CD UC
Presence/Absence Frequency Presence/Absence Frequency
Abdominal pain ✔ + ✔ +
Diarrhea ✔ + ✔ +
Hematochezia ✔/✗ +/− ✔/✗ +
Abdominal mass ✔ + ✔ +/−
Malnutrition ✔ + ✔/✗ +/−
Abdominal distension ✔/✗ +/− ✔/✗ +/−
Sub occlusive symptoms ✔ + ✗ -
Perianal disease ✔ +/− ✗ -
Fistulas ✔ +/− ✗ -
Anemia ✔ + ✔/✗ +/−
Iron deficiency ✔ + ✔/✗ +/−
Low vitamin D ✔ + ✔/✗ +/−
Elevated inflammatory markers ✔ + ✔/✗ +/−
✔ the symptoms/sign is present; ✗ the symptoms/sign is absent; ✔/✗ is present occasionally or during the acute phase of disease; + frequent; +/− variable; - absent.
For IBD, there are both pharmacological and non-pharmacological options to manage symptoms. Current drug treatments for IBD are aminosalicylates (5-ASA) that can be used in combination with steroids to induce and maintain remission [28][29]. If CD is mild to moderate, mesalamine is the first-line therapy while sulfasalazine is most effective at maintaining remission in UC [28][30]. The mainstay treatments of IBDs are hydrocortisone and prednisolone with glucocorticoid properties [28]. The preferred steroid is prednisolone, administered orally [28] (0.75–1 mg/kg of body weight) [5] and can be used in the short term to alleviate symptoms of moderate and severe CD [28]. Moreover, with a low dose of steroids, azathioprine may be introduced [28]; in fact, immune suppressants have been adapted for the treatment of IBD. Thiopurines (azathioprine, 6-mercaptopurine and methotrexate) are beneficial in 50 to 70% of patients [28] but are generally reserved for patients who are steroid resistant or steroid dependent [28][31]. Anti-TNF monotherapy is effective in maintaining remission [28], especially in patients with moderate–severe UC who have inadequate response or intolerance to conventional therapy [28][29].
A treatment which can prevent inflammation remains a cornerstone for IBD management and the diet also plays a pivotal role in the prevention of inflammatory bowel disease risk development [32][33]. The spread of the Western diet, rich in fats, protein, simple sugars and low in fruit and vegetables, represents a possible cause for the increase in IBD [34]. Indeed, diet affects intestinal inflammation through mechanisms such as the ability to present antigens and the alteration of the balance of prostaglandins (involved in the inflammatory pattern) and microbiota [35][36]. In particular, numerous studies have underlined the increased incidence of IBD due to excessive consumption of sugars or sugar-sweetened beverages [19][37], proteins (especially from red meat) [38], animal fats and linoleic acid. In fact, red meat consumption has been suggested to have a pro-inflammatory effect. This may be due to the cooking method and the concurrent presence of saturated fats that establish deleterious effects [19]. A high consumption of total fatty acids, polyunsaturated fatty acids (PUFAs), especially omega 6 fatty acids, increases the risk of developing both UC and CD [23]. The recent literature also shows that nutrition could influence the development of IBD [39] but actually few dietary recommendations exist. The American Journal of Gastroenterology published the American College of Gastroenterology (ACG) Practice Guidelines for CD and UC, which suggest eating frequent small meals or snacks every 3–4 h, drinking enough fluids to avoid dehydration, eating food with added probiotics and prebiotics and using multivitamins [40]. During remission, patients can include whole grains and a variety of fruits and vegetables in their daily eating plan; however, when there are symptoms, it is recommended to consume low-fiber foods [40]. Foods recommended for IBD are: low-fat and lactose-free milk and dairy products, lean and white meat, fish or eggs, grains with less than 2 g of fiber per serving, low-fiber vegetables and fruits (i.e., lettuce, strained vegetable juice, fruit juice without pulp, ripe banana or melons), less than eight teaspoons/day of oils and to drink water or beverages without caffeine [40]. The effect of alcohol in IBD is still controversial: some studies document positive effects of alcohol consumption in the development of UC [41][42] but this effect seems to be nullified if alcohol consumption is associated with cigarette smoking [43].

2. The Effect of Dietary Fibers in IBD

In the literature, since 1978, there has been considerable interest in dietary fibers as a therapeutic option in IBD but its role is unclear, with conflicting findings [44].
In the case of IBD, it is suggested that a diet rich in fibers, vitamin D and adequate consumption of citrus fruits has a protective role [39]. In fact, high consumption of fiber and fruit is associated with a 73–80% decreased risk of CD, while a high intake of vegetables reduces the risk of UC [23].
It is important to underline that patients with stricturing Crohn’s disease should be careful to their intake of dietary fiber and fibrous foods for symptomatic management of strictures and may need supplementation with enteral or parenteral nutritional requirements [45].
Although Anantakrishnan et al. observed that the consumption of at least 24.3 g of fiber per day (particularly fruit-derived fiber) reduces the risk of developing Crohn’s disease by 40% but not UC [46], in the literature, there are some conflicting evidence on the use of high-fiber foods in IBD. To date, it is clear that they are not recommended during flare-ups or during active disease states, fistulas or strictures [40]. In fact, in CD, a low-fiber diet should be used for a short period, and it is indicated only in certain conditions, such as acute relapses (with diarrhea and cramps), intestinal stenosis, bacterial proliferation of the small intestine and after some type of surgery [40]. In 2020, Day et al., in a systematic review, analyzed different study designs to determine the correct amount of dietary fiber in individuals with IBD [47]. They compared the adequacy of fiber intakes with that of a control group or compared to national dietary guidelines, and examined factors associated with fiber consumption [48]. They concluded that individuals with IBD are used to consuming less fiber than healthy populations and that fiber intakes are inadequate compared to national fiber guidelines [47].
It is also necessary to mention the role of fermentable carbohydrates, or FODMAPs (oligosaccharides, disaccharides, monosaccharides and fermentable polyols), in IBD. FODMAPs have an osmotic and fermentative action because they recall water and gas in the intestinal lumen being partially or completely indigestible [49]. A low-FODMAP diet is usually suggested in the case of Irritable Bowel Syndrome (IBS) that is characterized by symptoms such as abdominal pain, meteorism, bloating, diarrhea or constipation [50][51]. Approximately one-third of IBD patients complain of IBS-like intestinal symptoms in the absence of actual gastrointestinal inflammation, thus usually an overlap of symptoms has been recognized [52]. There are several studies that evaluate the association between IBD and consumption of FODMAPs. In a randomized controlled trial (RCT), improvements in gastrointestinal symptoms were observed in patients in remission or with mild–moderate disease and coexisting IBS-like symptoms after following a low-FODMAP diet for approximately 6 weeks [53]. Results showed a significant reduction in symptoms in the Low-FODMAP diet group compared to the No Diet group (p = 0.02) [53]. A further study evaluated the effect of FODMAP consumption in quiescent IBD patients allocated to a series of 3-day fermentable carbohydrate challenges in a random order (fructan: 12 g/die; galacto-oligosaccharides: GOS, 6 g/die; sorbitol: 6 g/die; and glucose placebo: 12 g/die), each separated by a washout period [54]. At the end of the study, the authors observed that fewer patients reported adequate relief of functional gastrointestinal symptoms (62.1%) compared to glucose (89.7%) (p = 0.033), and that fructans, but not GOS or sorbitol, exacerbated gastrointestinal functional symptoms [55]. However, it is necessary to carry out further studies to evaluate the effect of different types and doses of FODMAP in patients with IBD [54].

3. Side Effects of Dietary Fibers with a Focus on IBD

To date, the daily amount of dietary fiber is suggested by the EFSA, The American Heart Association Eating Plan and the Academy of Nutrition and Dietetics [56][57][58] but there is no tolerable upper limit for total fiber intake; thus, eating more fibers can cause uncomfortable side effects [59], such as constipation, intestinal blockage, bloating or diarrhea [60][61][62]. Inadequate hydration and reduced physical activity combined with high fiber consumption can induce constipation; fiber is not fully digested or excreted from the body, generating intestinal blockages. In this case, intestinal bacteria ferment these undigested fibers [63], producing gas [64] and leading to symptoms such as bloating and flatulence. One strategy to minimize intestinal gas production is to consume fibers gradually and not suddenly. On the other hand, excessive consumption of fibers, especially insoluble ones, can also lead to diarrhea [59][65].
Moreover, high fiber consumption can reduce the rate of gastrointestinal micronutrient absorption, especially calcium and iron [66]. This is due to the chemical and physical characteristics of fiber such as fermentation, bulking capacity, binding capacity, viscosity and gel formation, water retention capacity and solubility [67] and also to the presence of some compounds such as phytates, oxalates, and tannins [68]. This is a big issue for IBD patients, who are already malnourished for gastro-intestinal malabsorption, and are further destabilized.
IBD patients report intolerance to some types of fibers because they lack fermentative microbe activities compared to individuals with normal microbial fermentative activity [68]. The absence of these microbes makes the fibers indigestible and therefore intact; this fibers interact with host cell receptors and promote intestinal inflammation [68].
The study by Armstrong et al. investigated the role of unfermented β-fibers in fueling inflammation in IBD patients [69]. β-Fructans (inulin and oligofructose/FOS) are β-(2 → 1)-linked fructose oligo- and polysaccharides. They are abundant in plant sources such as chicory root, agave and artichokes, while less abundant in banana, wheat, onion and garlic [70].
In some IBD patients, β-fructan fibers have shown potential negative impacts. Indeed, dietary β-fructans induce inflammation through activation of TLR2 and NLRP332 pathways [71] and promote the production of reactive oxygen species (ROS) interacting with carbohydrate receptors (GLP-1R) [72][73].
Although inulin could present positive effects on inflammation, there are several studies that have shown that it exacerbates the severity of colitis in an IL10-/- and DSS model of colitis [74] and facilitates the progression of hepatocellular carcinoma in mice [75].
Moreover, it has been seen that the consumption of unfermented FOS could also induce the production of pro-inflammatory cytokines in peripheral blood mononuclear cells (PBMCs) and in THP-1 macrophages, and this was seen in biopsies from IBD patients [76][77].

5. Mechanism of Action of Dietary Fibers in IBD

Although current dietary guidelines are not so clear on the amount and the type of fiber that should be consumed in IBD [48][48], in the literature, several studies evaluated the effects of fermentable and non-fermentable fibers in IBD patients. It is clear that some fermentable fibers such as resistant starch (that is not digested in the small intestine) and inulin are metabolized by intestinal bacteria to SCFAs [55][55], acetate, butyrate and propionate, and they have immunomodulatory properties, promote the regeneration of the intestinal epithelium, lower the pH of the colon and inhibit the growth of pathogens [78][78].

The IBD-altered microbiota composition results in a lower production of anti-inflammatory and immunoregulatory metabolites, in particular butyrate, a lack of which may contribute to increase intestinal inflammation [19]. Butyrate plays a central role in the development of IBD because it represents the main energy substrate for colonocytes [79] and the alteration of its metabolism is linked with mucosal damage and inflammation [80]. In fact, the integration of some types of fibers (especially fermentable fibers) produces SCFAs capable of maintaining remission and reducing mucosal lesions [78]. In addiction, SFCAs, partic- ularly acetate and butyrate, balance mucus production and secretion. Mucus production at the level of the epithelium is a form of host protection to prevent microbial invasion and susceptibility to infection. A diet low in fiber produces less SFCAs and results in an increase in harmful metabolites that increases susceptibility of infections by deterio- ration of the mucus layer and contribute to the development of chronic disease and colorectal cancer (CRC) [80][81][82].chanism of Action of Dietary Fibers in IBD

Although current dietary guidelines are not so clear on the amount and the type of fiber that should be consumed in IBD [48], in the literature, several studies evaluated the effects of fermentable and non-fermentable fibers in IBD patients.

It is clear that some fermentable fibers such as resistant starch (that is not digested in the small intestine) and inulin are metabolized by intestinal bacteria to SCFAs [55], acetate, butyrate and propionate, and they have immunomodulatory properties, promote the regeneration of the intestinal epithelium, lower the pH of the colon and inhibit the growth of pathogens [78].

The IBD-altered microbiota composition results in a lower production of anti-inflammatory and immunoregulatory metabolites, in particular butyrate, a lack of which may contribute to increase intestinal inflammation [19]. Butyrate plays a central role in the development of IBD because it represents the main energy substrate for colonocytes [79] and the alteration of its metabolism is linked with mucosal damage and inflammation [80]. In fact, the integration of some types of fibers (especially fermentable fibers) produces SCFAs capable of maintaining remission and reducing mucosal lesions [78]. In addiction, SFCAs, partic- ularly acetate and butyrate, balance mucus production and secretion. Mucus production at the level of the epithelium is a form of host protection to prevent microbial invasion and susceptibility to infection. A diet low in fiber produces less SFCAs and results in an increase in harmful metabolites that increases susceptibility of infections by deterio- ration of the mucus layer and contribute to the development of chronic disease and colorectal cancer (CRC) [80][81][82].

5. Mechanism of Action of Dietary Fibers in IBD

Although current dietary guidelines are not so clear on the amount and the type of fiber that should be consumed in IBD , in the literature, several studies evaluated the effects of fermentable and non-fermentable fibers in IBD patients.

It is clear that some fermentable fibers such as resistant starch (that is not digested in the small intestine) and inulin are metabolized by intestinal bacteria to SCFAs  , acetate, butyrate and propionate, and they have immunomodulatory properties, promote the regeneration of the intestinal epithelium, lower the pH of the colon and inhibit the growth of pathogens  .

The IBD-altered microbiota composition results in a lower production of anti-inflammatory and immunoregulatory metabolites, in particular butyrate, a lack of which may contribute to increase intestinal inflammation [19]. Butyrate plays a central role in the development of IBD because it represents the main energy substrate for colonocytes [79] and the alteration of its metabolism is linked with mucosal damage and inflammation [80]. In fact, the integration of some types of fibers (especially fermentable fibers) produces SCFAs capable of maintaining remission and reducing mucosal lesions  [78]. In addiction, SFCAs, partic- ularly acetate and butyrate, balance mucus production and secretion. Mucus production at the level of the epithelium is a form of host protection to prevent microbial invasion and susceptibility to infection. A diet low in fiber produces less SFCAs and results in an increase in harmful metabolites that increases susceptibility of infections by deterio- ration of the mucus layer and contribute to the development of chronic disease and colorectal cancer (CRC) [80][81][82].

6. Conclusion

Diet plays a crucial role in the treatment of IBD; however, no dietary compo- nent is considered responsible for the disease [45]. Thus, patients with IBD should be advised to eat a varied diet that meets their energetic and nutrients requirements, including dietary fibers [45]. In the literature, it is clear that IBD subjects tend to consume less fiber than healthy controls [45]. Studies have shown that fiber supplementation alone is unlikely to restore IBD patients’ microbiota to a healthy state. IBD patients are more at risk of protein-energy malnutrition than the general popula- tion. They have difficulty in gaining weight and, especially those affected by CD, could have deficiencies in micronutrients such as iron, vitamin B12 and vitamin D [83][84] [85][86][87][88].

All of these nutritional problems also have a serious psychosocial repercussion and worsen patients’ quality of life [89]. In fact, a majority of individuals with IBD believe that specific foods trigger their disease flares, although this belief is not supported by any study [90].

This research evaluated the effects of dietary fibers in the two different types of IBD, Crohn’s disease and ulcerative colitis. Actually, there is no consensus on the type and the amount of dietary fibers to suggest in these two cases even when taking into consideration the phase of the disease. Further studies are necessary to determine the appropriate amount and type of fiber to suggest in the case of IBD.

This entry is adapted from the peer-reviewed paper 10.3390/nu14224775

References

  1. Agrawal, M.; Spencer, E.A.; Colombei, J.-F.; Ungaro, C. Approach to the Management of Recently Diagnosed Inflammatory Bowel Disease Patients: A User’s Guide for Adult and Pediatric Gastroenterologists. Gastroenterology 2021, 161, 47–65.
  2. Cohen, A.N.; Rubin, D.T. New Targets in Inflammatory Bowel Disease Therapy: 2021. Curr. Opin. Gastroenterol 2021, 37, 357–363.
  3. Zhao, M.; Gönczi, L.; Lakatos, P.L.; Burisch, J. The Burden of Inflammatory Bowel Disease in Europe in 2020. J. Crohn’s Colitis 2021, 15, 1573–1587.
  4. Flynn, S.; Eisenstein, S. Inflammatory Bowel Disease Presentation and Diagnosis. Surg. Clin. N Am. 2019, 99, 1051–1062.
  5. Ogura, Y.; Bonen, D.K.; Inohara, N.; Nicolae, D.L.; Chen, F.F.; Ramos, R.; Britton, H.; Moran, T.; Karaliuskas, R.; Duerr, R.H.; et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature 2001, 411, 603–606.
  6. Cadwell, K.; Liu, J.Y.; Brown, S.L.; Miyoshi, H.; Loh, J.; Lennerz, J.K.; Kishi, C.; Kc, W.; Carrero, J.A.; Hunt, S.; et al. A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells. Nature 2008, 456, 259–263.
  7. Krieg, A.; Correa, R.G.; Garrison, J.B.; Le Negrate, G.; Welsh, K.; Huang, Z.; Knoefel, W.T.; Reed, J.C. XIAP mediates NOD signaling via interaction with RIP2. Proc. Natl. Acad. Sci. USA 2009, 106, 14524–14529.
  8. Johansson, M.E.V.; Holmén Larsson, J.M.; Hansson, G.C. The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host-microbial interactions. Proc. Natl. Acad. Sci. USA 2011, 108, 4659–4665.
  9. Knights, D.; Silverberg, M.S.; Weersma, R.K.; Gevers, D.; Dijkstra, G.; Huang, H.; Tyler, A.D.; Van Sommeren, S.; Imhann, F.; Stempak, J.M.; et al. Complex host genetics influence the microbiome in inflammatory bowel disease. Genome Med. 2014, 6, 107.
  10. Travassos, L.H.; Carneiro, L.A.M.; Ramjeet, M.; Hussey, S.; Kim, Y.-G.; Magalhães, J.G.; Yuan, L.; Soares, F.; Chea, E.; Le Bourhis, L.; et al. Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. Nat. Immunol. 2009, 11, 55–62.
  11. Hampe, J.; Franke, A.; Rosenstiel, P.; Till, A.; Teuber, M.; Huse, K.; Albrecht, M.; Mayr, G.; De La Vega, F.M.; Briggs, J.; et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat. Genet. 2006, 39, 207–211.
  12. Lee, C.; Chang, E.B. Inflammatory Bowel Disease and the Microbiome: Searching the Crime Scene for Clues. Gastroenter-Ology 2021, 160, 524–537.
  13. Di Sabatino, A.; Di Stefano, M. Malattie del colon. In Medicina Interna Sistematica, 7th ed.; Edra Masson: Seregno, Italy, 2015; Volume 1, pp. 1316–1350.
  14. Petagna, L.; Antonelli, A.; Ganini, C.; Bellato, V.; Campanelli, M.; Divizia, A.; Efrati, C.; Franceschilli, M.; Guida, A.M.; Ingallinella, S.; et al. Pathophysiology of Crohn’s disease inflammation and recurrence. Biol. Direct 2020, 15, 23.
  15. Satsangi, J.; Silverberg, M.S.; Vermeire, S.; Colombel, J.-F. The Montreal classification of inflammatory bowel disease: Contro-versies, consensus, and implications. Gut 2006, 55, 749–753.
  16. Feuerstein, J.D.; Cheifetz, A.S. Crohn Disease: Epidemiology, Diagnosis, and Management. Mayo Clin. Proc. 2017, 92, 1088–1103.
  17. Pochini, L.; Galluccio, M.; Scalise, M.; Console, L.; Pappacoda, G.; Indiveri, C. OCTN1: A Widely Studied but Still Enigmatic Organic Cation Transporter Linked to Human Pathology and Drug Interactions. Int. J. Mol. Sci. 2022, 23, 914.
  18. Biancone, L.; Armuzzi, A. Malattia di Crohn. In UNIGASTRO: Malattie Dell’apparato Digerente, 9th ed.; Edra Masson: Trento, Italy, 2019; pp. 167–176.
  19. Wark, G.; Samocha-Bonet, D.; Ghaly, S.; Danta, M. The Role of Diet in the Pathogenesis and Management of Inflammatory Bowel Disease: A Review. Nutrients 2021, 13, 135.
  20. Veauthier, B.; Hornecker, J.R. Crohn’s Disease: Diagnosis and Management. Am. Fam. Physician 2018, 98, 661–669.
  21. Danese, S.; D’Amico, F.; Bonovas, S.; Peyrin-Biroulet, L. Positioning Tofacitinib in the Treatment Algorithm of Moderate to Severe Ulcerative Colitis. Inflamm. Bowel Dis. 2018, 24, 2106–2112.
  22. Heller, F.; Fromm, A.; Gitter, A.H.; Mankertz, J.; Schulzke, J. Epithelial apoptosis is a prominent feature of the epithelial barrier disturbance in in-testinal inflammation: Effect of proinflammatory interleukin-13 on epithelial cell function. Mucosal Immunol 2008, 1 (Suppl. S1), S58–S61.
  23. Hou, J.K.; Abraham, B.; El-Serag, H. Dietary Intake and Risk of Developing Inflammatory Bowel Disease: A Systematic Review of the Literature. Am. J. Gastroenterol 2011, 106, 563–573.
  24. Wilkins, T.; Jarvis, K.; Patel, J. Diagnosis and management of Crohn’s disease. Am. Fam. Physician 2011, 84, 1365–1375.
  25. Nakase, H.; Uchino, M.; Shinzaki, S.; Matsuura, M.; Matsuoka, K.; Kobayashi, T.; Saruta, M.; Hirai, F.; Hata, K.; Hiraoka, S.; et al. Evidence-based clinical practice guidelines for inflammatory bowel disease 2020. J. Gastroenterol 2021, 56, 489–526.
  26. Du, L.; Ha, C. Epidemiology and Pathogenesis of Ulcerative Colitis. Gastroenterol Clin. N. Am. 2020, 49, 643–654.
  27. Kucharzik, T.; Koletzko, S.; Kannengiesser, K.; Dignass, A. Ulcerative Colitis-Diagnostic and Therapeutic Algorithms. Dtsch. Arztebl Int. 2020, 117, 564–574.
  28. Pithadia, A.B.; Jain, S. Treatment of inflammatory bowel disease (IBD). Pharmacol. Rep. 2011, 63, 629–642.
  29. Raine, T.; Bonovas, S.; Burisch, J.; Kucharzik, T.; Adamina, M.; Annese, V.; Bachmann, O.; Bettenworth, D.; Chaparro, M.; Czuber-Dochan, W.; et al. ECCO Guidelines on Therapeutics in Ulcerative Colitis: Medical Treatment. J. Crohn’s Colitis 2021, 16, 2–17.
  30. Lichtenstein, G.R.; Loftus, E.V.; Isaacs, K.L.; Regueiro, M.D.; Gerson, L.B.; Sands, B.E. ACG clinical guideline: Management of Crohn’s disease in adults. Am. J. Gastroenterol 2018, 113, 481–517.
  31. Korelitz, B.I.; Adler, D.J.; Mendelsohn, R.A.; Sacknoff, A.L. Long-term experience with 6-mercaptopurine in the treatment of Crohn’s disease. Am. J. Gastroenterol 1993, 88, 1198–1205.
  32. Campmans-Kuijpers, M.J.E.; Dijkstra, G. Food and Food Groups in Inflammatory Bowel Disease (IBD): The Design of the Groningen Anti-Inflammatory Diet (GrAID). Nutrients 2021, 13, 1067.
  33. Gerasimidis, K.; Godny, L.; Sigall-Boneh, R.; Svolos, V.; Wall, C.; Halmos, E. Current recommendations on the role of diet in the aetioliogy and management of IBD. Frontline Gastroenterol 2021, 13, 160–167.
  34. Amre, D.K.; D’Souza, S.; Morgan, K.; Seidman, G.; Lambrette, P.; Grimard, G.; Israel, D.; Mack, D.; Parviz, G. Imbalances in dietary consumption of fatty acids, vegetables, and fruits are associ-ated with risk for Crohn’s disease in children. Am. J. Gastroenterol. 2007, 102, 2016–2025.
  35. De Filippo, C.; Cavalieri, D.; Di Paola, M.; Ramazzotti, M.; Poullet, J.B.; Massart, S.; Collini, S.; Pieraccini, G.; Lionetti, P. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc. Natl. Acad. Sci. USA 2010, 107, 14691–14696.
  36. Sharon, P.; Ligumsky, M.; Rachmilewitz, D.; Zor, U. Role of prostaglandins in ulcerative colitis. Enhanced production during ac-tive disease and inhibition by sulfasalazine. Gastroenterology 1978, 75, 638–640.
  37. Ahsan, M.; Koutroumpakis, F.; Rivers, C.R.; Wilson, A.S.; Johnston, E.; Hashash, J.G.; Barrie, A.; Alchoufete, T.; Babichenko, D.; Tang, G.; et al. High Sugar-Sweetened Beverage Consumption Is Associated with Increased Health Care Utilization in Patients with Inflammatory Bowel Disease: A Multiyear, Prospective Analysis. J. Acad. Nutr. Diet. 2022, 122, 1488–1498.e1.
  38. Dong, C.; Mahamat-Saleh, Y.; Racine, A.; Jantchou, P.; Chan, S.; Hart, A.; Carbonnel, F.; Boutron-Ruault, M.C. OP17 Protein intakes and risk of inflammatory bowel disease in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC-IBD). J. Crohn’s Colitis 2020, 14, S015.
  39. Owczarek, D.; Rodacki, T.; Domagała-Rodacka, R.; Cibor, D.; Mach, T. Diet and nutritional factors in inflammatory bowel diseases. World, J. Gastroenterol. 2016, 22, 895–905.
  40. Brown, A.C.; Rampertab, S.D.; Mullin, G. Existing dietary guidelines for Crohn’s disease and ulcerative colitis. Expert Rev. Gastroenterol. Hepatol. 2011, 5, 411–425.
  41. Nakamura, Y.; Labarthe, D.R. A case-control study of ulcerative colitis with relation to smoking habits and alcohol consump-tion in Japan. Am. J. Epidemiol. 1994, 140, 902–911.
  42. Jiang, L.; Xia, B.; Li, J.; Ye, M.; Deng, C.; Ding, Y.; Luo, H.; Ren, H.; Hou, X.; Liu, H. Risk factors for ulcerative colitis in a Chinese population: An age-matched and sex-matched case-control study. J. Clin. Gastroenterol. 2007, 41, 280–284.
  43. El-Tawil, A.M. Epidemiology and inflammatory bowel diseases. World J. Gastroenterol. 2013, 19, 1505–1507.
  44. Grosse, C.S.J.; Christophersen, C.T.; Devine, A.; Lawrance, I.C. The role of a plant-based diet in the pathogenesis, etiology and management of the inflammatory bowel diseases. Expert Rev. Gastroenterol. Hepatol. 2020, 14, 137–145.
  45. Lamb, C.A.; Kennedy, N.A.; Raine, T.; Hendy, P.A.; Smith, P.J.; Limdi, J.K.; Hayee, B.; Lomer, M.C.E.; Parkes, G.C.; Selinger, C.; et al. British Society of Gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults. Gut 2019, 68 (Suppl. S3), s1–s106.
  46. Ananthakrishnan, A.N.; Khalili, H.; Konijeti, G.G.; Higuchi, L.M.; de Silva, P.; Korzenik, J.R.; Fuchs, C.S.; Willett, W.C.; Rich-ter, J.M.; Chan, A.T. A prospective study of long-term intake of dietary fiber and risk of Crohn’s disease and ulcerative colitis. Gastroenterology 2013, 145, 970–977.
  47. Day, A.S.; Davis, R.; Costello, S.P.; Yao, C.K.; Andrews, J.M.; Bryant, R.V. The Adequacy of Habitual Dietary Fiber In-take in Individuals with Inflammatory Bowel Disease: A Systematic Review. J. Acad. Nutr. Diet. 2021, 121, 688–708.e3.
  48. Stephen, A.M.; Champ, M.M.-J.; Cloran, S.J.; Fleith, M.; Van Lieshout, L.; Mejborn, H.; Burley, V.J. Dietary fibre in Europe: Current state of knowledge on definitions, sources, recommendations, intakes and relationships to health. Nutr. Res. Rev. 2017, 30, 149–190.
  49. Whelan, K.; Martin, L.D.; Staudacher, H.; Lomer, M.C.E. The low FODMAP diet in the management of irritable bowel syndrome: An evidence-based review of FODMAP restriction, reintroduction and personalisation in clinical practice. J. Hum. Nutr. Diet. 2018, 31, 239–255.
  50. Halpin, S.J.; Ford, A.C. Prevalence of Symptoms Meeting Criteria for Irritable Bowel Syndrome in Inflammatory Bowel Disease: Systematic Review and Meta-Analysis. Am. J. Gastroenterol. 2012, 107, 1474–1482.
  51. Lacy, B.E.; Mearin, F.; Chang, L.; Chey, W.D.; Lembo, A.J.; Simren, M.; Spiller, R. Bowel disorders. Gastroenterology 2016, 150, 1393–1407.e5.
  52. Fairbrass, K.M.; Costantino, S.J.; Gracie, D.J.; Ford, A.C. Prevalence of irritable bowel syndrome-type symptoms in patients with inflammatory bowel disease in remission: A systematic review and meta-analysis. Lancet Gastroenterol. Hepatol. 2020, 5, 1053–1062.
  53. Pedersen, N.; Ankersen, D.V.; Felding, M.; Végh, Z.; Burisch, J.; Abstract, P.M. Mo1210 Low FODMAP Diet Reduces Irritable Bowel Symptoms and Improves Quality of Life in Patients with Inflammatory Bowel Disease in a Randomized Controlled Trial. Gastroenterology 2014, 146, 58.
  54. Cox, S.R.; Prince, A.C.; Myers, C.E.; Irving, P.M.; Lindsay, J.O.; Lomer, M.C.; Whelan, K. Fermentable Carbohydrates Exacerbate Functional Gastrointestinal Symptoms in Patients with Inflammatory Bowel Disease: A Randomised, Double-blind, Placebo-controlled, Cross-over, Re-challenge Trial. J. Crohn’s Colitis 2017, 11, 1420–1429.
  55. Schmoldt, A.; Benthe, H.F.; Haberland, G. Towards a food pharmacy: Immunologic modulation through diet. Biochem Phar-Macol 1975, 24, 1639–1641.
  56. European Food Safety Authority. Scientific opinion on dietary reference values for carbohydrates and dietary fibre. EFSA J. 2010, 8, 1462.
  57. Van Horn, L. Fiber, lipids, and coronary heart disease. A statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation 1997, 95, 2701–2704.
  58. Dahl, W.J.; Stewart, M.L. Position of the Academy of Nutrition and Dietetics: Health Implications of Dietary Fiber. J. Acad. Nutr. Diet. 2015, 115, 1861–1870.
  59. Grabitske, H.A.; Slavin, J.L. Gastrointestinal Effects of Low-Digestible Carbohydrates. Crit. Rev. Food Sci. Nutr. 2009, 49, 327–360.
  60. Lesbros-Pantoflickova, D.; Michetti, P.; Fried, M.; Beglinger, C.; Blum, A.L. Meta-analysis: The treatment of irritable bowel syndrome. Aliment. Pharmacol. Ther. 2004, 20, 1253–1269.
  61. Rees, G.; Davies, J.; Thompson, R.; Parker, M.; Liepins, P. Randomised-controlled trial of a fibre supplement on the symptoms of irritable bowel syndrome. J. R. Soc. Promot. Health 2005, 125, 30–34.
  62. Bijkerk, C.J.; Muris, J.W.M.; Knottnerus, J.A.; Hoes, A.W.; De Wit, N.J. Systematic review: The role of different types of fibre in the treatment of irritable bowel syndrome. Aliment. Pharmacol. Ther. 2004, 19, 245–251.
  63. Goodlad, R.A. Dietary fibre and the risk of colorectal cancer. Gut 2001, 48, 587–589.
  64. Gonlachanvit, S.; Coleski, R.; Owyang, C.; Hasler, W. Inhibitory actions of a high fibre diet on intestinal gas transit in healthy volunteers. Gut 2004, 53, 1577–1582.
  65. Eswaran, S.; Muir, J.; Chey, W.D. Fiber and Functional Gastrointestinal Disorders. Am. J. Gastroenterol. 2013, 108, 718–727.
  66. Bosscher, D.; Van Caillie-Bertrand, M.; Van Cauwenbergh, R.; Deelstra, H. Availabilities of calcium, iron, and zinc from dairy infant formulas is affected by soluble dietary fibers and modified starch fractions. Nutrition 2003, 19, 641–645.
  67. Brownlee, I.A. The physiological roles of dietary fibre. Food Hydrocoll. 2011, 25, 238–250.
  68. Slavin, J. Fiber and Prebiotics: Mechanisms and Health Benefits. Nutrients 2013, 5, 1417–1435.
  69. Armstrong, H.K.; Bording-Jorgensen, M.; Santer, D.M.; Zhang, Z.; Valcheva, R.; Rieger, A.M.; Sung-Ho, K.J.; Dijk, S.I.; Mahmood, R.; Ogungbola, O.; et al. Unfermented β-fructan fibers fuel inflammation in select inflammatory bowel disease patients. Gastroenterology 2022, 29, S0016–S5085.
  70. Mitmesser, S.; Combs, M. Chapter 23-Prebiotics: Inulin and Other Oligosaccharides; Floch, M.H., Ringel, Y., Allan Walker, W., Eds.; The Microbiota in Gastrointestinal Pathophysiology; Academic Press: Cambridge, MA, USA, 2017; pp. 201–208.
  71. Singh, V.; Yeoh, B.S.; Walker, R.; Xiao, X.; Saha, P.; Golonka, R.M.; Cai, J.; Bretin, A.C.A.; Cheng, X.; Liu, Q.; et al. Microbiota fermentation-NLRP3 axis shapes the impact of dietary fibres on intestinal inflammation. Gut 2019, 68, 1801–1812.
  72. Speert, D.P.; Eftekhar, F.; Puterman, M.L. Nonopsonic phagocytosis of strains of Pseudomonas aeruginosa from cystic fibrosis patients. Infect. Immun. 1984, 43, 1006–1011.
  73. Kim, K.-J.; Park, J.-M.; Lee, J.-S.; Kim, Y.S.; Kangwan, N.; Han, Y.-M.; Kang, E.A.; An, J.M.; Park, Y.K.; Hahm, K.-B. Oligonol prevented the relapse of dextran sulfate sodium-ulcerative colitis through enhancing NRF2-mediated antioxidative defense mechanism. J. Physiol. Pharmacol. Off. J. Pol. Physiol. Soc. 2018, 69, 3.
  74. Miles, J.P.; Zou, J.; Kumar, M.-V.; Pellizzon, M.; Ulman, E.; Ricci, M.; Gewirtz, A.T.; Chassaing, B. Supplementation of Low- and High-fat Diets with Fermentable Fiber Exacerbates Severity of DSS-induced Acute Colitis. Inflamm. Bowel Dis. 2017, 23, 1133–1143.
  75. Singh, V.; Yeoh, B.S.; Chassaing, B.; Xiao, X.; Saha, P.; Aguilera Olvera, R.; Lapek, J.D., Jr.; Zhang, L.; Wang, W.; Hao, S.; et al. Dysregulated microbial fermentation of sol-uble fiber induces cholestatic liver cancer. Cell 2018, 175, 679–694.e22.
  76. Zhang, J.; Fu, S.; Sun, S.; Li, Z.; Guo, B. Inflammasome activation has an important role in the development of spontaneous colitis. Mucosal Immunol. 2014, 7, 1139–1150.
  77. Coccia, M.; Harrison, O.J.; Schiering, C.; Asquith, M.J.; Becher, B.; Powrie, F.; Maloy, K.J. IL-1beta mediates chronic intestinal inflammation by promoting the accumula-tion of IL-17A secreting innate lymphoid cells and CD4(+) Th17 cells. J. Exp. Med. 2012, 209, 1595–1609.
  78. Pituch-Zdanowska, A.; Banaszkiewicz, A.; Albrecht, P. The role of dietary fibre in inflammatory bowel disease. Gastroenterol. Rev. 2015, 10, 135–141.
  79. Champ, M.M. Physiological aspects of resistant starch and in vivo measurements. J. AOAC Int. 2004, 87, 749–755.
  80. Salvi, P.S.; Cowles, R.A. Butyrate and the Intestinal Epithelium: Modulation of Proliferation and Inflammation in Homeosta-sis and Disease. Cells 2021, 10, 1775.
  81. Windey, K.; De Preter, V.; Verbeke, K. Relevance of protein fermentation to gut health. Mol. Nutr. Food Res. 2012, 56, 184–196.
  82. Johansson, M.E.V.; Phillipson, M.; Petersson, J.; Velcich, A.; Holm, L.; Hansson, G.C. The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria. Proc. Natl. Acad. Sci. USA 2008, 105, 15064–15069.
  83. Lomer, M.C.; Hart, A.L.; Verjee, A.; Daly, A.; Solomon, J.; Mclaughlin, J. What are the dietary treatment research priorities for inflammatory bowel disease? A short report based on a priority setting partnership with the James Lind Alliance. J. Hum. Nutr. Diet. 2017, 30, 709–713.
  84. Gerasimidis, K.; Nichols, B.; McGowan, M.; Svolos, V.; Papadopoulou, R.; Kokkorou, M.; Rebull, M.; Bello Gonzalez, T.; Han-sen, R.; Russell, R.K.; et al. The Effects of Commonly Consumed Dietary Fibres on the Gut Microbiome and Its Fibre Fermentative Capacity in Adults with Inflammatory Bowel Disease in Remission. Nutrients 2022, 14, 1053.
  85. Mijac, D.D.; Janković, G.L.; Jorga, J.; Krstić, M.N. Nutritional status in patients with active inflammatory bowel disease: Prev-alence of malnutrition and methods for routine nutritional assessment. Eur. J. Intern Med. 2010, 21, 315–319.
  86. Høivik, M.L.; Reinisch, W.; Cvancarova, M.; Moum, B. IBSEN study group. Anaemia in inflammatory bowel disease: A pop-ulation-based 10-year follow-up. Aliment. Pharm. Ther. 2014, 39, 69–76.
  87. Ward, M.G.; Kariyawasam, V.C.; Mogan, S.B.; Patel, K.V.; Pantelidou, M.; Sobczyńska-Malefora, A.; Porté, F.; Griffin, N.; Anderson, S.H.C.; Sanderson, J.D.; et al. Prevalence and risk factors for functional vitamin B12 deficiency in patients with Crohn’s disease. Inflamm Bowel Dis. 2015, 21, 2839–2847.
  88. Suibhne, T.N.; Cox, G.; Healy, M.; O’Morain, C.; O’Sullivan, M. Vitamin D deficiency in Crohn’s disease: Prevalence, risk fac-tors, and supplement use in an outpatient setting. J. Crohns Colitis 2012, 6, 182–188.
  89. Czuber–Dochan, W.; Morgan, M.; Hughes, L.D.; Lomer, M.C.E.; Lindsay, J.O.; Whelan, K. Perceptions and psychosocial impact of food, nutrition, eating and drinking in people with inflammatory bowel disease: A qualitative investigation of food–related quality of life. J. Hum. Nutr. Diet. 2020, 33, 115–127.
  90. Vagianos, K.; Shafer, L.A.; Witges, K.; Graff, L.A.; Targownik, L.E.; Bernstein, C.N. Self-reported flares among people living with inflammatory bowel disease are associated with stress and worry but not associated with recent diet changes: The Manitoba Living with IBD Study. JPEN J. Parenter Enter. Nutr. 2022, 46, 1686–1698.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
This entry is offline, you can click here to edit this entry!
ScholarVision Creations
Feedback